Abstract

Reduced exercise capacity is common in people with chronic obstructive pulmonary diseases (COPD) and chronic smokers and is suggested to be related to skeletal muscle dysfunction. Previous studies using human muscle biopsies have shown fiber-type shifting in chronic smokers particularly those with COPD. These results, however, are confounded with aging effects because people with COPD tend to be older. In the present study, we implemented an acute 7-day cigarette smoke-exposed model using Sprague-Dawley rats to evaluate early effects of cigarette smoking on soleus muscles. Rats (n = 5 per group) were randomly assigned to either a sham air (SA) or cigarette smoking (CS) groups of three different concentrations of total particulate matters (TPM) (CSTPM2.5, CSTPM5, CSTPM10). Significantly lower percentages of type I and higher type IIa fiber were detected in the soleus muscle in CS groups when compared with SA group. Of these, only CSTMP10 group exhibited significantly lower citrate synthase activity and higher muscle tumor necrosis factor-α level than that of SA group. Tumor necrosis factor-α level was correlated with the percentage of type I and IIa fibers. However, no significant between-group differences were found in fiber cross-sectional area, physical activities, or lung function assessments. In conclusion, acute smoking may directly trigger the onset of glycolytic fiber type shift in skeletal muscle independent of aging.

Highlights

  • [6] exercise intolerance in people with chronic obstructive pulmonary disease (COPD) may not be solely due to the intrapulmonary changes associated with lung disease, and by systemic extra-pulmonary changes induced by smoking

  • To address whether significant lung function impairment occurred following a 7-day acute smoking protocol, we investigated a battery of respiratory variables and lung mechanics

  • Our results showed that there was no significant change in main effects or any Time x Group interactions for any of the respiratory variables among the four exposure groups of different total particulate matters (TPM) (Fig 1)

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Summary

Introduction

Cigarette smoking on muscle fiber type derangement level of exercise capacity than non-smokers. [6] exercise intolerance in people with COPD may not be solely due to the intrapulmonary changes associated with lung disease, and by systemic extra-pulmonary changes induced by smoking. Peripheral skeletal muscle dysfunction has been hypothesized as one of the key factors contributing to reduced exercise capacity. [9, 14] As mentioned previously, smoking is the primary contributing factor for the development of COPD Individuals diagnosed with this condition usually report a long smoking history and have the disease diagnosed when they are older. This makes it difficult to determine if smoking induces early detrimental effects on locomotor muscle. The direct and early effects of smoking on muscle fiber type distribution and muscle atrophy, as measured by cross-sectional area, remain unclear

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